山姜素对肺微血管内皮细胞损伤保护机制

Protection Mechanism of Alpinetin on Pulmonary Microvascular Endothelial Cells Injury

目的研究山姜素对急性人肺微血管内皮细胞(human pulmonary microvascular endothelial cells,HPMECs)损伤的保护机制。方法应用不同浓度的LPS(0.01、0.1、1.0、10 mg/L)作用于HPMECs,确定造模最佳浓度。应用山姜素(40、80、160、320 mg/L)干预HPMECs损伤模型,另选择正常HPMECs为对照组,每组3个重复样本,观察各组HPMECs存活率,检测细胞间黏附分子-1(intercellular cell adhesion molecule-1,ICAM-1)、TNF-α、水通道蛋白-1(APQ-1)蛋白及mRNA表达。结果与对照组比较,模型组ICAM-1及TNF-α蛋白表达升高,AQP-1蛋白及mRNA表达降低(P<0.05)。与模型组比较,80、160 mg/L山姜素组细胞存活率升高,ICAM-1及TNF-α蛋白表达降低,AQP-1蛋白及mRNA表达升高(P<0.05,P<0.01)。结论山姜素通过下调ICAM-1、TNF-α蛋白表达并上调APQ-1蛋白及mRNA表达,从而对急性HPMECs损伤起保护作用。

Objective To explore the protection mechanisms about Alpinetin to acute human pul- monary microvascular endothelial cells （HPMECs） injury. Methods Different concentration of LPS （0.01,0.1,1.0,10 mg/L） was applied to the HPMECs to induce acute HPMECs injury. The HPMECs mod- els （n =3） were intervened by Alpinetin（40,80,160,320 mg/L） . Normal HPMECs were selected as con- trol group. The viability of HPMECs was observed,mRNA and protein expression of intercellular cell adhe- sion molecule-1 （ ICAM-1 ） ,TNF-α,APQ-1 were detected. Results Compared with control group, the pro- tein expression of ICAM-1, TNF-α were increased, the protein and mRNA expression of APQ-1 and the vi- ability of HPMECs were decreased in model group （P 〈0.05）. Compared with model group,ICAM-1 and TNF-α protein expressions were significantly inhibited in Alpinetin （80,160 mg/L） group, the mRNA and protein expression of APQ-1 and the viability of HPMECs were significantly increased （P 〈0.05, P 〈 0.01 ）. Conclusion Alpenitin could protect the HPMECs injury by down-regulated protein expression of ICAM-1, TNF-α and up-regulated the mRNA and protein expression of APQ-1.